Segiet W, Krieter H, Stieber C, Albrecht D M, van Ackern K
Institute of Anesthesiology, Faculty for Clinical Medicine Mannheim, University of Heidelberg, Germany.
Intensive Care Med. 1995 Oct;21(10):817-25. doi: 10.1007/BF01700965.
To assess the effects of the cyclooxygenase inhibitor diclofenac in a canine model of pulmonary occlusion and reperfusion of the left lower lobe (LLL).
Twelve adult beagle dogs (13-17 kg) were randomly assigned to a control group (n = 6) and a diclofenac-treated group (n = 6). Animals in the treatment group received 20 mg diclofenac sodium/kg as a single dose both before the experiment and at the end of surgical preparation; six animals served as controls.
In the anesthetized animals, the left upper and middle lobes were resected. Circulation and ventilation of the LLL were selectively blocked by clamping. Complete occlusion of the LLL (30 min) was followed by periods of selective reperfusion (10 min, RP) and combined reperfusion and reventilation (120 min, RP/RV).
Reperfusion of the LLL resulted in a significant increase in pulmonary arterial pressure (Ppa) in the early RP/RV period as compared to baseline values (25.3 +/- 4.7 vs 15.8 +/- 1.9 mmHg, p < 0.05, paired t-test). This increase was significantly inhibited in the diclofenac-treated animals (17.0 +/- 2.0 mmHg, p < 0.01 vs controls, ANOVA). Gravimetrically determined extravascular lung water (EVLW) showed no significant difference in the continuously ventilated lobes of the right lung between diclofenac-treated animals (3.8 ml/g dry weight) and controls (3.9 +/- 0.9 ml/g dry weight) at the end of the experiment. EVLW, however, increased significantly in the LLL of control animals after 2 h of combined reperfusion and reventilation, whereas this increase was significantly inhibited in the diclofenac-treated animals (4.5 +/- 0.7 ml/g dry weight in the diclofenac group vs 6.5 +/- 1.3 ml/g dry weight in the control group, p < 0.05).
Diclofenac inhibits the increase in both pulmonary arterial pressure and EVLW during reperfusion and reventilation of LLL. Thus, these changes appear to be mediated by cyclooxygenase metabolites.
评估环氧化酶抑制剂双氯芬酸在犬左下叶肺阻塞及再灌注模型中的作用。
12只成年比格犬（13 - 17千克）被随机分为对照组（n = 6）和双氯芬酸治疗组（n = 6）。治疗组动物在实验前及手术准备结束时均接受20毫克双氯芬酸钠/千克的单次剂量；6只动物作为对照。
在麻醉的动物中，切除左上叶和中叶。通过夹闭选择性阻断左下叶的循环和通气。左下叶完全阻塞30分钟后，进行选择性再灌注（10分钟，RP）以及再灌注与再通气联合操作（120分钟，RP/RV）。
与基线值相比，左下叶再灌注在再灌注与再通气早期导致肺动脉压（Ppa）显著升高（25.3±4.7对15.8±1.9毫米汞柱，p < 0.05，配对t检验）。这种升高在双氯芬酸治疗的动物中受到显著抑制（17.0±2.0毫米汞柱，与对照组相比p < 0.01，方差分析）。实验结束时，通过重量法测定的血管外肺水（EVLW）在双氯芬酸治疗动物的右肺持续通气叶与对照组（3.9±0.9毫升/克干重）之间无显著差异。然而，在再灌注与再通气联合操作2小时后，对照组动物的左下叶EVLW显著增加，而在双氯芬酸治疗的动物中这种增加受到显著抑制（双氯芬酸组为4.5±0.7毫升/克干重，对照组为6.5±1.3毫升/克干重，p < 0.05）。
双氯芬酸可抑制左下叶再灌注和再通气期间肺动脉压及EVLW的升高。因此，这些变化似乎是由环氧化酶代谢产物介导的。
